Summary of Study ST003043
This data is available at the NIH Common Fund's National Metabolomics Data Repository (NMDR) website, the Metabolomics Workbench, https://www.metabolomicsworkbench.org, where it has been assigned Project ID PR001894. The data can be accessed directly via it's Project DOI: 10.21228/M8WQ6G This work is supported by NIH grant, U2C- DK119886.
See: https://www.metabolomicsworkbench.org/about/howtocite.php
This study contains a large results data set and is not available in the mwTab file. It is only available for download via FTP as data file(s) here.
Study ID | ST003043 |
Study Title | Retinoic acid receptor alpha activity in proximal tubules prevents kidney injury and fibrosis |
Study Summary | Retinoid levels of all-trans-retinol, retinoic acid, and retinyl palmitate were measured in the kidney and serum of GCERRARaD (kidney proximal tubule RARalpha knockout mice) females 3 days or 3 months post-tamoxifen (n=5/group) and age-matched Wild Type females (n=4). |
Institute | Weill Cornell Medicine |
Last Name | Tang |
First Name | Xiao-Han |
Address | 1300 York Ave, New York, NY10065 |
xit2001@med.cornell.edu | |
Phone | 3478327329 |
Submit Date | 2024-01-14 |
Raw Data Available | Yes |
Raw Data File Type(s) | mzML |
Analysis Type Detail | LC-MS |
Release Date | 2024-01-18 |
Release Version | 1 |
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Project:
Project ID: | PR001894 |
Project DOI: | doi: 10.21228/M8WQ6G |
Project Title: | Retinoid levels measurement in kidney and serum |
Project Type: | MS analysis |
Project Summary: | Chronic kidney disease (CKD) is characterized by a gradual loss of kidney function and affects ca. 13.4% of the global population. Progressive tubulointerstitial fibrosis, driven in part by proximal tubule (PT) damage, is a hallmark of late stages of CKD and contributes to the development of kidney failure, for which there are limited treatment options. Normal kidney development requires signaling by vitamin A (retinol), which is metabolized to retinoic acid (RA), an endogenous agonist for the retinoic acid receptors (RAR alpha, beta, gamma). RARalpha levels are decreased in a mouse model of diabetic nephropathy (DN) and restored with RA administration; additionally, RA treatment reduces fibrosis. We developed a mouse model in which a spatiotemporal (tamoxifen-inducible) deletion of RARalpha in kidney PT cells of adult mice causes mitochondrial dysfunction, massive PT injury, and apoptosis without the use of additional nephrotoxic substances. Long-term effects (3-4.5 months) of RARalpha deletion include increased PT secretion of transforming growth factor beta (TGF-beta1), inflammation, interstitial fibrosis, and decreased kidney function, all of which are major features of human CKD. Therefore, RARalpha’s actions in proximal tubules (PTs) are crucial for PT homeostasis, and loss of RARalpha causes injury and a key CKD phenotype. |
Institute: | Weill Cornell Medicine |
Last Name: | Tang |
First Name: | Xiao-Han |
Address: | 1300 Yates Avenue, New York, NY 10065 |
Email: | xit2001@med.cornell.edu |
Phone: | 3478327329 |
Publications: | DiKun KM et al, RETINOIC ACID RECEPTOR a ACTIVITY IN PROXIMAL TUBULES PREVENTS KIDNEY INJURY AND FIBROSIS. PNAS, 2024. |